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HYPERSENSITIVITY REACTIONS

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Title: HYPERSENSITIVITY REACTIONS


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HYPERSENSITIVITY REACTIONS
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TYPE 3 HYPERSENSITIVITY REACTION
  • Type III hypersensitivity is also known as immune
    complex hypersensitivity
  • Reaction may be general (e.g., serum sickness) or
    may involve individual organs including skin
    (e.g., systemic lupus erythematosus, Arthus
    reaction), kidneys (e.g., lupus nephritis), lungs
    (e.g., Aspergillus), blood vessels (e.g.,
    Polyarteritis), joints (e.g., rheumatoid
    arthritis) or other organs
  • This reaction may be the pathogenic mechanism of
    diseases caused by many microorganisms

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  • The reaction may take 3 - 10 hours after exposure
    to the antigen (as in Arthus reaction)
  • They are mostly of the IgG class, although IgM
    may also be involved
  • The antigen may be exogenous (chronic bacterial,
    viral or parasitic infections), or endogenous
    (non-organ specific autoimmunity e.g., systemic
    lupus erythematosus, SLE)

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  • Primary components are soluble immune complexes
    and complement (C3a, 4a and 5a)
  • The damage is caused by platelets and neutrophils
  • The lesion contains primarily neutrophils and
    deposits of immune complexes and complement
  • Macrophages infiltrating in later stages may be
    involved in the healing process

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  • A local type III hypersensitivity reaction can be
    triggered in the skin of sensitized individuals
    who possess IgG antibodies against the
    sensitizing antigen.
  • When antigen is injected into the skin,
    circulating IgG antibody that has diffused into
    the tissues forms immune complexes locally.
  • The immune complexes bind Fc receptors on mast
    cells and other leukocytes, which creates a local
    inflammatory response with increased vascular
    permeability.

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  • The enhanced vascular permeability allows fluid
    and cells, especially polymorphonuclear
    leukocytes, to enter the site from the local
    vessels.
  • This reaction is called an Arthus reaction
  • The immune complexes also activate complement,
    releasing C5a, which contributes to the
    inflammatory reaction by ligating C5a receptors
    on leukocytes

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  • A systemic type III hypersensitivity reaction,
    known as serum sickness, can result from the
    injection of large quantities of a poorly
    catabolized foreign antigen
  • This illness was so named because it frequently
    followed the administration of therapeutic horse
    antiserum

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  • Serum sickness occurs 710 days after the
    injection of the horse serum, an interval that
    corresponds to the time required to mount a
    primary immune response that switches from IgM to
    IgG antibody against the foreign antigens in
    horse serum
  • The clinical features of serum sickness are
    chills, fever, rash, arthritis, and sometimes
    glomerulonephritis
  • Urticaria is a prominent feature of the rash,
    implying a role for histamine derived from
    mast-cell degranulation
  • In this case the mast-cell degranulation is
    triggered by the ligation of cellsurface Fc?RIII
    by IgG-containing immune complexes

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  • An injection of a foreign protein or proteins
    leads to an antibody response. These antibodies
    form immune complexes with the circulating
    foreign proteins. The complexes are deposited in
    small vessels and activate complement and
    phagocytes, inducing fever and the symptoms of
    vasculitis, nephritis, and arthritis. All these
    effects are transient and resolve when the
    foreign protein is cleared.

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TYPE 4 HYPERSENSITIVITY REACTION
  • Type IV hypersensitivity is also known as cell
    mediated or delayed type hypersensitivity
  • The classical example of this hypersensitivity is
    tuberculin (Montoux) reaction which peaks 48
    hours after the injection of antigen (PPD or old
    tuberculin)
  • The lesion is characterized by induration and
    erythema

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  • Type IV hypersensitivity is involved in the
    pathogenesis of many autoimmune and infectious
    diseases (tuberculosis, leprosy, blastomycosis,
    histoplasmosis, toxoplasmosis, leishmaniasis,
    etc.) and granulomas due to infections and
    foreign antigens
  • Another form of delayed hypersensitivity is
    contact dermatitis (poison ivy (figure 6),
    chemicals, heavy metals, etc.) in which the
    lesions are more papular
  • Type IV hypersensitivity can be classified into
    three categories depending on the time of onset
    and clinical and histological presentation

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DELAYED HYPERSENSITIVITY REACTION- 3 types
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  • Mechanisms of damage in delayed hypersensitivity
    include T lymphocytes and monocytes and/or
    macrophages
  • Cytotoxic T cells (Tc) cause direct damage
    whereas helper T (TH1) cells secrete cytokines
    which activate cytotoxic T cells and recruit and
    activate monocytes and macrophages, which cause
    the bulk of the damage
  • The delayed hypersensitivity lesions mainly
    contain monocytes and a few T cells
  • Major lymphokines involved in delayed
    hypersensitivity reaction include monocyte
    chemotactic factor, interleukin-2,
    interferon-gamma, TNF alpha/beta, etc.

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  • Diagnostic tests in vivo include delayed
    cutaneous reaction (e.g. Montoux test (figure 5))
    and patch test (for contact dermatitis)
  • In vitro tests for delayed hypersensitivity
    include mitogenic response, lympho-cytotoxicity
    and IL-2 production

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